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Microbiology · General microbiology and sterilisation: porin loss
Sample itemDuring therapy of Pseudomonas aeruginosa pneumonia, the isolate becomes resistant to imipenem but stays susceptible to ceftazidime and piperacillin-tazobactam. No carbapenemase is detected. Which mechanism is most likely?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
D. Loss of the OprD outer membrane porin
Imipenem enters Pseudomonas through the OprD porin. Mutational loss of OprD lowers imipenem uptake and gives resistance while other beta-lactams that use different routes remain active.
Option by option
A. Acquisition of the altered PBP2a
PBP2a is the methicillin-resistance protein of Staphylococcus aureus, not Pseudomonas.
B. Ribosomal methylation by an erm gene
erm methylation causes macrolide-lincosamide-streptogramin resistance and not beta-lactam resistance.
C. Production of an extended-spectrum beta-lactamase
An ESBL hydrolyses cephalosporins such as ceftazidime and spares carbapenems.
D. Loss of the OprD outer membrane porin (correct)
Correct. Loss of OprD reduces imipenem entry and selectively raises its MIC.
Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.
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